Improvement of sepsis-related acute lung injury through Naringin by regulating TGF-β1/Smad2 signaling pathway
Objective To investigate the protective effect of naringenin on acute lung injury related with sepsis;To discuss its possible mechanism.Methods Totally 30 male SD rats were randomly divided into sham-operation group,model group,naringin low-,medium-and high-dosage groups,with 6 rats in each group.The sepsis-related acute lung injury model was established by cecal ligation and puncture in all groups except the sham-operation group.After modeling,naringin low-,medium-and high-dosage groups were given naringin 20 mg/kg,40 mg/kg and 80 mg/kg,respectively for gavage,while the sham-operation group and the model group were given the same volume of distilled water by gavage,once a day,for 2 days.Pathological changes in lung tissue were observed using HE staining.The levels of 1L-1,IL-6 and IL-18 in bronchoalveolar lavage fluid(BALF)were measured by ELISA;the expression of TNF-α in lung tissue was detected by immunofluorescence histopathology;the expressions of TGF-β1,TGF-βR1 and Smad2 were detected by Western Blot.An agonist group and a naringin plus agonist group were set up,with 6 mice in each group,and the expressions of TGF-β1 and Smad2 protein in the lung tissue of each group were detected by immunohistochemical staining to verify the effect of naringin on the expressions of TGF-β1 and Smad2 protein.Results Compared with the model group,the pathological injury of lung tissue in naringin groups were obviously alleviated,and the levels of IL-1β,IL-6 and IL-18 in BALF decreased(P＜0.01),the protein expressions of TNF-α,TGF-β1,TGF-βR1 and Smad2 in lung tissue decreased(P＜0.01 or P＜0.05).Further verification found that the expressions of TGF-β1 and Smad2 in the agonist group increased(P＜0.01),while the expressions of TGF-β1 and Smad2 in the naringin agonist group decreased(P＜0.01).Conclusion Naringin can reduce the inflammatory response in the lung of the rats to protect against sepsis-related acute lung injury,and its protective effect could be related to the inhibition of the TGF-β1/Smad2 signaling pathway.
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